Evidence map›Paper›PMID 28091829›Full record

ArticleInflammation2017

Inhibition of DPP-4 Activity and Neuronal Atrophy with Genistein Attenuates Neurological Deficits Induced by Transient Global Cerebral Ischemia and Reperfusion in Streptozotocin-Induced Diabetic Mice.

Mithun Singh Rajput, Purnima Dey Sarkar, Nilesh Prakash Nirmal

Abstract read
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Article in Inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Mithun Singh RajputDepartment of Medical Biochemistry, Mahatma Gandhi Memorial Medical College, A.B. Road, Indore, 452001, M.P., India. mithun.sgsits@gmail.com.
Purnima Dey SarkarDepartment of Medical Biochemistry, Mahatma Gandhi Memorial Medical College, A.B. Road, Indore, 452001, M.P., India.
Nilesh Prakash NirmalCenter for Nutrition and Food Sciences, Queensland Alliance for Agriculture and Food Innovation, Health and Food Sciences Precinct, University of Queensland, Block 10, 39 Kessels Road, Coopers Plains, Acherfield Brisbane, QLD, 4108, Australia.
Mahatma Gandhi Memorial Medical College · INAgriculture and Food · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genistein, an isoflavonoid phytoestrogen, has been known for its potential pharmacological properties especially for neuroprotection and treating diabetes. The present study aims to determine the neuroprotective efficacy of genistein against global cerebral ischemia-reperfusion-induced neuronal injury in streptozotocin-induced diabetic mice and explore the underlying mechanisms. Streptozotocin-induced diabetic mice were subjected to transient cerebral ischemia by occluding both common carotid arteries for 30 min followed by 24 h reperfusion to induce neuronal injury. Effect of genistein (2.5, 5.0, and 10.0 mg/kg, i.p., o.d.) treatment on ischemia-reperfusion-induced neuronal injury in diabetic mice was evaluated in terms of cerebral infarct size, oxidative damage, mitochondrial activity in terms of neuronal apoptosis and cellular viability, dipeptidyl peptidase-4 activity and active glucagon-like peptide-1 concentration, and neurological functions measured as short-term memory and motor performance. Genistein administration following transient cerebral ischemia significantly (p ˂ 0.0001) counteracted cognitive impairment and re-established (p ˂ 0.001) motor performance in diabetic mice. Ischemia-reperfusion increased the infarct size, genistein administration prevented the increase in cerebral infarct size (p ˂ 0.0001) and significantly suppressed (p ˂ 0.001) the increase in cerebral oxidative stress in transient cerebral ischemia-reperfusion subjected diabetic mice. Genistein treatment significantly (p ˂ 0.001) reduced neuronal apoptosis and increased cellular viability (p ˂ 0.0001), almost completely suppressed (p ˂ 0.0001) the circulating dipeptidyl peptidase-4 activity, and enhanced (p ˂ 0.0001) glucagon-like peptide-1 concentration in diabetic mice with cerebral ischemia-reperfusion. This study suggests that genistein has potent neuroprotective activity against global cerebral ischemia-reperfusion-induced neuronal injury and consequent neurological deficits in streptozotocin-induced diabetic mice.

Indexed as

AtrophyAnimalsBrain IschemiaCell SurvivalCognitive DysfunctionDiabetes Mellitus, ExperimentalDipeptidyl Peptidase 4GenisteinMiceNeuronsNeuroprotective AgentsReperfusion InjuryDipeptidyl Peptidase 4Dpp4 protein, mouseGenisteinNeuroprotective Agentsbrain atrophycerebral ischemiaDPP-4genisteinGLP-1mitochondrial function

Identifiers

PMID28091829
OpenAlexW2575666808

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.